scholarly journals The Comparison of Tnf α (Tumor Necrosis Factor α) Serum Levels Between Cytotoxin - Associated Gene A (Caga) Positive and Negative in Patients with Gastritis Helicobacter pylori

Author(s):  
Fitri Armanti Karo ◽  
Leonardo Basa Dairi ◽  
Gontar Alamsyah Siregar
1995 ◽  
Vol 132 (6) ◽  
pp. 668-672 ◽  
Author(s):  
Ismail Çelik ◽  
Sema Akalin ◽  
Tomris Erbaş

Çelik I, Akalin S, Erbaş T. Serum levels of interleukin 6 and tumor necrosis factor-α in hyperthyroid patients before and after propylthiouracil treatment. Eur J Endocrinol 1995;132:668–72. ISSN 0804–4643 Contrary to the usual inhibitory role of tumor necrosis factor-α (TNF-α) thyroid metabolism, it also has specific stimulatory effects in autoimmune thyroid disorders, including induction of HLA class II antigen-presenting cell—T cell interaction. Despite high intrathyroidal concentrations, various studies were not able to demonstrate high serum levels of TNF-α in patients with Graves' disease. To investigate this discrepancy we determined TNF-α and interleukin 6 (IL-6) levels in 25 hyperthyroid patients who responded to propylthiouracil treatment (16 with Graves' disease and nine with toxic multinodular goiter) and compared them with the levels found in euthyroid patients with simple diffuse goiter (n = 15) and normal healthy controls (n = 15). Median IL-6 levels were high in both Graves' disease and toxic multinodular goiter patients before propylthiouracil treatment (23 and 26.5 pg/ml, respectively). After restoring euthyroidism there was a statistically significant decline to near-normal levels (3 and 10 pg/ml, respectively). On the other hand, median serum TNF-α levels were high only in Graves' disease patients (20 pg/ml) and could not be normalized with antithyroid medication (20 pg/ml) compared to that of controls (5 pg/ml). Tumor necrosis factor-α, but not IL-6, was found to be high in the sera of Graves' disease patients when euthyroid, which may be due to an ongoing antigen–antibody interaction, a feature of autoimmune attack. It remains to be determined whether the degree of TNF-α and/or IL-6 elevation will be a predictor of disease recurrence. Ismail Çelik, Section of Oncology, Dept. of Medicine, Hacettepe University Institute of Oncology, Ankara 06100, Turkey


2015 ◽  
Vol 6 (5) ◽  
pp. 12-16
Author(s):  
Shiv Kumar Yadav ◽  
Qi Jian YI

Objective: To investigate the changes in serum levels of ghrelin, tumor necrosis factor-α and interleukin-6 in Children with Congenital Heart Disease (CHD) at pre and post percutaneous management of the lesions. Material & Methods: We measured the serum levels of ghrelin, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) by enzyme linked immunosorbent assays (ELISA) in 67 patients with CHD and in 20 control subjects; and compared these markers of inflammatory reaction between groups of pre-closure (37 patients) and at the end of 5 minutes (37 patients), 1 month (22 patients) and 3 month (8 patients) post percutaneous management of the lesions. Results: Our results showed that the patients with CHD had significantly higher serum level of Ghrelin, TNF-α and IL-6 in comparison of the controls but gradually return towards the baseline levels at the end of 3 months post percutaneous management of the lesions. Conclusion: The inflammatory reaction is activated in pre-closure and self-limited post-closure in children with CHD. Percutaneous management could improve the inflammatory process, which is safe and effective in children with CHD.DOI: http://dx.doi.org/10.3126/ajms.v6i5.12129 Asian Journal of Medical Sciences Vol.6(5) 2015 12-16   


1993 ◽  
Vol 48 (3) ◽  
pp. 324-331 ◽  
Author(s):  
Didier Hober ◽  
Bertrand Roblin ◽  
Robert Vergez-Pascal ◽  
Gerard Granic ◽  
Michele Maniez-Montreuil ◽  
...  

2019 ◽  
Vol 88 ◽  
pp. 149-150 ◽  
Author(s):  
Erkoseoglu Ilknur ◽  
Kadioglu Mine ◽  
Cavusoglu Irem ◽  
Sisman Mulkiye ◽  
Aran Turhan ◽  
...  

2017 ◽  
Vol 9 ◽  
pp. 117957351770927 ◽  
Author(s):  
Rudy Chang ◽  
Kei-Lwun Yee ◽  
Rachita K Sumbria

Tumor necrosis factor α (TNF-α) plays a central role in the pathophysiology of Alzheimer’s disease (AD). Food and Drug Administration–approved biologic TNF-α inhibitors are thus a potential treatment for AD, but they do not cross the blood-brain barrier. In this short review, we discuss the involvement of TNF-α in AD, challenges associated with the development of existing biologic TNF-α inhibitors for AD, and potential therapeutic strategies for targeting TNF-α for AD therapy.


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